Beyond SHM and CSR: AID and related cytidine deaminases in the host response to viral infection

Adv Immunol. 2007;94:215-44. doi: 10.1016/S0065-2776(06)94007-3.

Abstract

As the primary effector of immunoglobulin somatic hypermutation (SHM) and class switch recombination (CSR), activation-induced cytidine deaminase (AID) serves an important function in the adaptive immune response. Recent advances have demonstrated that AID and a group of closely related cytidine deaminases, the APOBEC3 proteins, also act in the innate host response to viral infection. Antiviral activity was first attributed to APOBEC3G as a potent inhibitor of HIV. It is now apparent that the targets of the APOBEC3 proteins extend beyond HIV, with family members acting against a wide variety of viruses as well as host-encoded retrotransposable genetic elements. Although it appears to function through a different mechanism, AID also possesses antiviral properties. Independent of its antibody diversification functions, AID protects against transformation by Abelson murine leukemia virus (Ab-MLV), an oncogenic retrovirus. Additionally, AID has been implicated in the host response to other pathogenic viruses. These emerging roles for the AID/APOBEC cytidine deaminases in viral infection suggest an intriguing evolutionary connection of innate and adaptive immune mechanisms.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Cytidine Deaminase / immunology*
  • HIV Infections / immunology
  • Humans
  • Immunoglobulin Class Switching
  • Somatic Hypermutation, Immunoglobulin
  • Virus Diseases / immunology*

Substances

  • AICDA (activation-induced cytidine deaminase)
  • Cytidine Deaminase